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He used to be an upstanding member of cell society. He was the head of the PTA, for goodness sake! But, life got rough, and he broke down. He couldn’t handle the stresses that came his way, so he took himself out of the game, but not completely (suicide was never his style). Now, the Heckler stands on the sidelines, watching as all the other cells do the kinds of things he used to do: divide, communicate, build.

Over time, he gets more and more bitter, and there comes a point where he’s no longer content to simply watch. So, he starts to heckle. He develops a heckler’s toolkit, which he calls SASP, that includes Screaming, Arguing, Spitting, and Provoking – all with the goal of destroying the health and happiness surrounding cells. Because if he can’t be a functioning member of society, why can they?

What is happening inside my body?

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Cellular senescence is a hallmark of aging characterized by the accumulation of badly damaged cells that are no longer able to divide or contribute to supporting the organism but also haven’t been killed. Normally, when a cell becomes dysfunctional, it destroys itself through a process of programmed cell death called apoptosis. As we get older, our immune system weakens, resulting in more and more cells avoiding apoptosis to live in this in-between state called senescence.

The problem with senescent cells is that they secrete a cocktail of harmful chemicals called SASP (senescence-associated secretory phenotype) that causes serious inflammation, damaging the cells and tissues around them.

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Why this matters to you

As your cells undergo stress, they can lose their ability to divide. They can also become zombies in the body that infect other cells, and the inflammation can add up, causing major systemic issues.

How HOP Box Helps: Quercetin, fisetin, berberine, and vitamin K2 all have roles in decreasing the number of senescent cells in our bodies (“The Hecklers”), both by preventing their formation and promoting their removal.

Learn about the other Downfalls of Aging

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Telomere Attrition
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Genomic Instability
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Epigenetic Alteration
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Loss of Proteostasis
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Cellular Senescence
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Mitochondrial Dysfunction
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Deregulated Nutrient Sensing
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Altered Intercellular Communication
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Stem Cell Exhaustion